AB0536 CORRECTION OF OMEGA-3 FATTY ACID DEFICIENCY AND IMPROVEMENT IN DISEASE ACTIVITY IN SLE PATIENTS TREATED WITH A CONCENTRATED EXTRACT OF KRILL OIL (AKM-3031)
Authors: J. E. Salmon, D. J. Wallace, V. Rus, P. Lipsky
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Omega-3 fatty acids play a critical role in regulating inflammation. Patients with SLE have been reported to be deficient in omega-3 fatty acids, and deficiency could play a role in the ongoing inflammation characteristic of this disease. Previous work has produced conflicting results regarding the capacity of Omega-3 supplementation to control SLE disease activity. <h3>Objectives</h3> The goals of this study were to determine the level of omega-3 deficiency in SLE patients and to determine whether supplementation with a concentrated extract of krill oil rich in omega-3 fatty acids (AKBM-3031) could overcome the deficiency in SLE patients and decrease disease activity. <h3>Methods</h3> This was a randomized double blind controlled multicenter study of patients with active SLE (SLEDAI &gt;/= 6). Patients meeting entry criteria were randomized to receive AKBM-3031 (4 grams/day) or identical placebo capsules containing mixed oils simulating that in a western diet (NCT03626311). Patients received investigational product or placebo daily for 24 weeks, at which time placebo patients could opt to receive AKBM-3031 for the subsequent 24 weeks, whereas those receiving AKBM-3031 continued on the medication. The primary outcome was the correction of the red blood cell omega-3 index determined by OmegaQuant. Changes in clinical features and adverse events were collected throughout the trial. <h3>Results</h3> 79 subjects were enrolled in the study; 97% of the patients were women and 56% were of European and 35% of African Ancestry. At baseline, the mean omega-3 index was 4.65+/- 1.09, below the lower limits of normal for the North American population (6.0). After 4 weeks of treatment with AKBM-3031, the Omega-3 index significantly increased from 4.65+/- 1.09 to 7.21+/-1.37, (p &lt; 0.0001), whereas no significant change was noted in the patients receiving placebo. Increases in the Omega-3 index in AKBM-3031 treated patients persisted throughout the 48 weeks of the trial. Notably, when patients were changed from placebo to AKBM-3031 at 24 weeks, there was a rapid increase in the Omega-3 index (4.62+/-1.39 to 6.58+/- 1.85, p=0.0001). The total number of adverse events was less in the AKMB-3031group (186) than in the placebo group (342), most were mild or moderate and no serious adverse events were noted. Although there were no significant changes in disease activity when the entire groups were examined, there was a significant decrease in disease activity measured by SLEDAI-2K at 4, 8 and 16 weeks (p=0.0007, 0.04, 0.02, respectively) in the patients receiving AKBM-3031with high disease activity at baseline (SLEDAI &gt;/=9). <h3>Conclusion</h3> Treatment of SLE patients with AKBM-3031 rapidly corrects the Omega-3 deficiency characteristic of these patients. AKBM-3031 was safe and decreased disease activity in those with more active SLE. These results suggest benefit of Omega-3 deficiency correction with AKBM-3031 in SLE patients with active disease and warrant a more extensive evaluation. <h3>Acknowledgements:</h3> This work was support by Aker Biomarine <h3>Disclosure of Interests</h3> None Declared.